Abstract
Lymphocytes are mobile and travel from blood to lymph and then return to blood, which ensures a coordinated expression of immunological functions. In lymph nodes (LN) and Peyer's patches, the port of entry for naive T and B cells is the high endothelial venules (HEVs). The endothelial cells of HEVs are characterized by the luminal presentation of various adhesion molecules and chemokines. Some of the endothelial adhesion molecules are responsible for the tissue-specific trafficking of lymphocytes by giving lymphocytes positional cues, and hence are called vascular addressins. The peripheral LN addressins (PNAd) include several sialomucins and the mucosal LN addressin is MAdCAM-1. The complementary lymphocyte homing receptors for these addressins are L-selectin for PNAd, and α4β7 integrin for MAdCAM-1. While L-selectin and their counter-receptors are primarily involved in lymphocyte rolling along the endothelial surface, LFA-1 and its counter-receptor ICAMs are thought to be involved in firm adhesion of lymphocytes. During the course of rolling, lymphocytes are rapidly and transiently activated by chemokines expressed in HEV, which leads to rapid activation of LFA-1-mediated lymphocyte adhesion to HEV. How the subsequent transmigration of lymphocytes is controlled remains poorly characterized. Here We briefly review the molecular mechanisms controlling chemokine-driven lymphocyte trafficking across HEVs.
